The Nutritional Importance of Coenzyme Q as a Dietary Supplement

Antioxidants are an important group of molecules that can keep us young and healthy. It has been postulated that these antioxidants can reduce the spread of cancer, reduce destructive Low Density Lipoproteins (LDL) in the blood, and provide a general protection for our cells (2,6). Coenzyme Q10, CoQ10, is considered to be one of these important antioxidants. It is well known that CoQ10 is essential in the mitochondria, and serves as the electron shuttle for Complex I, II, & IV. The benefits outside the mitochondria, and the effects of general health will be investigated in this report.

This report will be divided into three general sections. The first focus for this report will be the process of uptake of dietary CoQ10 (1,2,4,6). The second will involve the research done on the use of CoQ10 as a useful and required molecule outside the mitochondria. Heart disease, neurological defects, and limiting oxidation of LDL are health risks that may benefit from CoQ10 supplementation (3,5). The final focus of this review will be to examine the practical uses as a dietary supplement (4,6). There are many different reports stating a positive response to the dietary uptake of CoQ10, and other articles that are definitely not enthusiastic about the effectiveness, or safety, of this particular supplement (3,6,7).

Two of the reports reviewed dealt directly with CoQ10 uptake in rats from dietary supplements. In one study researchers examined where dietary uptake of vitamin E and coenzyme Q10, administered either separately or together, would occur in the rats’ tissues (1). Vitamin E was found to reach a plateau in the liver and plasma rather quickly, and accumulated slowly in other organs (heart, kidney, muscle, and brain). The increase of CoQ10 was observed in the liver and plasma, but no significant increase was recorded in the other organs. Researchers propose this discrepancy in uptake, of the CoQ10, may be due to the metabolic use of this vitamin as a precursor to other metabolites. They were also interested in the interaction between the two vitamins when supplemented simultaneously. It was found that excess vitamin E significantly increased the uptake of CoQ10; deficient vitamin E and CoQ10 in excess did not affect the uptake of vitamin E. CoQ10 has been proposed as a regenerator of vitamin E. When cellular situations call for the use of vitamin E somehow it needs to be regenerated. If CoQ10 is important in this process, then this would explain the increased absorption of CoQ10 into the tissues when excess vitamin E is present. The lack of additional CoQ10 uptake when vitamin E is deficient shows that CoQ10 is not a substitute antioxidant for vitamin E, but is involved in separate reactions. It was found that vitamin E decreases slowly in all tissues but in comparison, CoQ10 decreases at a relatively faster rate. This rapid disappearing act may be due to the metabolic use of CoQ10, or just effective maintenance by the tissues. All cells produce their own CoQ10, utilization of external sources is not necessary, and therefore the breakdown of dietary CoQ10 occurs quite rapidly.

A second group of researchers studied just the uptake of coenzyme Q10 in rats (2). The liver and plasma basal levels begin with low levels of CoQ10, but increased rapidly and steadily with administration of the dietary supplement. The spleen contained a significant amount of CoQ10 prior to adding the supplement, possibly due to the increased amount of blood in this organ, and levels increased at an even pace during the trial. No appreciable uptake was observed in the kidney and heart. The kidney and heart are postulated to have their own regulatory system for CoQ10 production and use, and do not use CoQ10 from the plasma.

The coenzyme Q10 was administered directly to the stomach, and from the value recovered in the tissues, it was estimated that only 2-3% of the supplemented CoQ10 was actually absorbed into the tissues (2). A possible reason for lack of intake into tissues indicates that CoQ10 plays a more diverse role in the plasma, than in cellular function. By centrifuging the cells from the liver they were able to determine which organelles the coenzyme targeted. The organelles with the highest concentration of CoQ10 were in the mitochondria and lysosomes. This makes a great deal of sense since Coenzyme Q10 is essential in the electron transport chain, which is a major function of these organelles.

Due to its chemical structure, CoQ10 is an ideal electron carrier in the cell wall lipid bilayer. It is both fat soluble, yet small enough to move about; thus it acts as a shuttle of electrons between immobile proteins. The structure consists of ten isoprenoid units and a benzoquinone. It is able to "shuttle" two electrons around between donors and acceptors.

One such system is the peroxidation of Low Density Lipoproteins. People at risk for coronary heart disease have a greater susceptibility towards LDL oxidation. Alleva et al found that supplementation with CoQ10 and vitamin E reduced the overall oxidation of LDL (3). It was noted though that the presence of other lipids, such as polyunsaturated fatty acids, reduced the effectiveness of CoQ10 as an antioxidant. This is possibly due to the "consumption of antioxidants" by these additional lipids (3).

Atherosceorolosis is another contributing factor towards heart disease. The inhibition of molecules that assist in causing platelet aggregation and plaque along the arterial walls would help alleviate this risk. A Texas trial on swine supplemented with CoQ10 found that an "antiaggregatory effect on platelets" is observed (4). The swine model is effective since the heart and circulatory systems are comparatively similar to those in humans. Serum levels were found to rise steadily for CoQ10 in most tissues as also noted in the previous experiments. In addition to the CoQ10 measurements, various other molecules associated with the on-set of heart disease were measured. It was found that some of these proaggregatory molecules decreased, thereby decreasing the opportunity for causing serious harm to the myocardial arteries (4).

Rabbits induced with Symptomatic Cerebral vasospasm, a tightening of the arteries, were treated with CoQ10 immediately after the hemorrhage was induced (5). Ischemic lesions, areas of tissue lacking oxygen from the depravation of blood, induced by an artificial blood clotting mechanism were prevented from causing permanent damage by the supplementation of Coenzyme Q10. The researchers found that rabbits induced with hemorrhaging in the brain survived and were neurologically unharmed when they were nutritionally supplemented with CoQ10. The researchers imply that the hemorrhaging, and blood clotting occur because of LDL being oxidized, and that aggravates the effects of the blood clot (5). This is prevented from happening with the CoQ10. Without the nutritional supplement the rabbits inevitably develop neurological disorders and may die.

A group of researchers in Denmark was interested in various dietary supplements as effective blockers of DNA damage. They took a group of smokers and gave them various levels and combinations of vitamin E, ascorbic acid, and/or coenzyme Q10. Their purpose for this research was to challenge/support the idea that fresh fruit and vegetables are more effective cancer fighting agents then the nutritional supplements by themselves (6). They used an accepted biomarker of DNA damage, 8-oxo-7,8-dihydro-2’-deoxyguanosine (8-oxodG), which is excreted in the urine. Mutation of DNA from a guanine to a thymine occurs in most cases because of oxidative damage to the guanine base. The mutated p53 suppressor gene is commonly found with the "guanine-thymine transversion" in lung cancer tissue(6). 8-oxodG is a marker for this type of mutation and is used as a marker for high risk cancer candidates

It was noted that most of the groups experienced increases in their plasma level of their respective supplement, except for the vitamin E and slow release ascorbic acid combination(6). A decrease in the expected plasma levels was observed for both supplements. As a side note, the researchers decided to toss the data from this group, but in my opinion it would have lent some credibility on their conjuncture that fresh fruit and vegetables are the more effective antioxidant due to the multiplicity of nutrients and antioxidants contained in them. Prieme et al found that no significant change in 8-oxodG was observed during the trial for any of their smokers using their combination of nutritional supplements, and concluded that the three supposed antioxidants were ineffective in reducing the risk of cancer.

The physical benefits of coenzyme Q10 was questioned, and tested on endurance athletes. Their aerobic capacity, and any observable physical improvement was measured before and after supplementation. There was a significant increase of CoQ10 in the blood serum after taking a capsule for 30 days. No significant improvement in aerobic or physical activity was observed. This is inconsistent with literature cited in the article that supports improved physical activity after supplementation. Possible explanations given were: inadequate dosage, or the possibility athletes naturally have sufficient CoQ10, and do not benefit from additional supplementation(3).

A possibly dangerous effect reported in Lancet is an interaction between a prescribed drug and easily available coenzyme Q10. It was reported that patients taking warfarin for heart embolisms were adversely affected by supplementation of CoQ10. It affected the concentration of the prescribed drug by lowering the serum concentration to an ineffective level(7). Warfarin is generally prescribed as an anticoagulant, and serum levels are important in tracking the effectiveness of the drug. Excess warfarin could cause uncontrolled internal bleeding, and not enough would be useless.

The benefit implied by researchers is that CoQ10 supplementation was most noticeable in serum activity. It can facilitate the prevention of atheroscleorosis(3,4). Damage to cell walls during hemorrhaging is lessened and even prevented with supplementation, as shown with the rabbits(5). As illustrated earlier plasma level intake is significant. For those deficient in CoQ10, either from age or other reasons, it would be prudent to supplement the diet with coenzyme Q10. It is absorbed into the blood quickly and could be available to cells at a rapid rate(1,3).

Coenzyme Q10 is indisputably an important coenzyme that we can not live without. It is an important component to cellular and plasma activity. The prevention of additional damage to, and assisting in, arterial cell wall recovery could be significant. The mechanism by which coenzyme Q10 functions needs to be investigated in greater depth to be able to maximize the use of this supplement. Much of what is known about its’ mechanism, function and benefit is conjecture and not proven fact. With careful planning and testing, researchers will unlock the secret of coenzyme Q10.

REFERENCES:

1. Zhang Y; Turunen M; Appelkvist EL. (1996) J Nutr 126, 2089-2097
2. Zhang Y; Aberg F; Appelkvist EL; Dallner G; Ernster L. (1995) J Nutr 125, 446-453
3. Weston SB; Ahou S; Weatherby RP; Robson SJ. (1997) Int J Sport Nutr 3, 197-206
4. Serebruany VL; Herzog WR; Atamas SP; Gurbel PA; Rohde M; Mortensen SA; Folker K. (1996) J Cardiovasc Pharmacol 28, 175-181
5. Alleva R; Tomasetti M; Battino M; Curatola G; Littarru GP; Folkers K. (1995) Proc. Natl. Acad. Sci USA 92, 9388-9391
6. Prieme H; Loft S; Nyyssonen K; Salonen JT; Poulsen HE. (1997) Am J Clin Nutr 65, 503-507
7. Spigset O. (1994) The Lancet 344, 1372-1373